Endocrine Abstracts

Introduction: Primary hyperparathyroidism (PHPT) is characterized by parathyroid hormone (PTH) overproduction, causing hypercalcemia. The most common cause is a parathyroid adenoma. PHPT most frequently presents as asymptomatic hypercalcemia or with nonspecific symptoms. Less frequently, it presents with the classical manifestations of bone disease and nephrolithiasis. Acute pancreatitis (AP) as the initial manifestation of PHPT has been reported rarely. Hypercalcemia can cause AP by leading to pancreatic calculi and ductal obstruction, and by activating trypsinogen to trypsin, causing pancreatic autodigestion.

Case Report: A 37 year-old man was admitted to the hospital due to AP. Initial tests revealed elevated amylase and lypase levels (164U/l [NR 13-53U/l] and 106U/l [NR 13-60U/l], respectively), hypercalcemia (14.9 mg/dl [NR 8.6-10.2 mg/dl]), hypophosphatemia (1.9 mg/dl [NR 2.5-4.5 mg/dl]) and acute kidney failure. Further investigation showed elevated serum PTH (1241 pg/ml [NR 14-72 pg/ml]), suggesting PHPT. During hospitalization, the patient was treated with IV fluids and pamidronate 90 mg. On discharge, calcemia was 10.3 mg/dl, amylase was 34U/l, lypase was 66U/l and renal function was normal. The patient denied any previous history of bone disease, nephrolithiasis or other symptoms of hypercalcemia. Renal ultrasound excluded kidney stones. To evaluate for the presence of multiple endocrine neoplasia syndromes types 1 and 2, pituitary function, calcitonin and plasma metanephrines were measured, which were normal. 99mTc-Sestamibi scintigraphy identified a 15 mm right inferior parathyroid nodule, therefore the patient underwent right inferior parathyroidectomy. Intraoperative PTH level decreased to 7 pg/ml. Histology revealed a parathyroid adenoma as the etiology of PHPT. The patient was discharged under calcium carbonate and cholecalciferol treatment (6000 mg + 1600UI per day). Laboratory tests in the first postoperative appointment showed normal PTH, calcium and phosphorus values (71 pg/ml, 9.7 mg/dl and 3.2 mg/dl, respectively). Levels remain normal after having suspended calcium and cholecalciferol therapy (59 pg/ml, 9.6 mg/dl and 2.7 mg/dl, respectively). There has been no recurrence of pancreatitis.

Discussion and Conclusions: AP in patients with PHPT is uncommon (estimated prevalence: 1%-13%), however this can be the initial manifestation of PHPT. While hypercalcemia causes under 1% of AP cases, in patients where calcemia is elevated, investigation of endocrine causes such as PHPT should be prompted. It is also important to note that although histology in this case suggested parathyroid adenoma, the patient presented with severe hypercalcemia (> 14 mg/dl) and very high serum PTH (≥ 10-12 times the upper limit of normal), which are potential predictive factors of parathyroid carcinoma (versus benign causes of PHPT). Therefore, close monitoring will be required.